Septicemia with its frequently lethal complications is one of the clinical syndromes in medicine feared most. It is therapeutically not controllable, claiming a few 100,000 casualties a year alone in the Western countries. New treatment options have to be looked for as antibiotics act too slowly, not preventing the release of bacterial toxins, partly even intensifying it. Pouring out of messenger substances (cytokines) by the host organism released by bacterial toxins is the most important element of the pathogenetic cascade leading to the clinical picture of septicemia. Various new therapeutic approaches, on the one hand, blocking of bacterial lipopolysaccharide (LPS) as the most important toxin by antibodies or antagonizing the endogenous, so-called proinflammatory cytokines failed completely in comprehensive clinical studies (C. Natanson et al., Ann. Intern Med. 120, 771–783 (1994).